Cytomegalovirus in the Neonate: Immune Correlates of Infection and Protection

Table 1

Summary of innate immune responses and their proposed role in control of or susceptibility to congenital CMV infection.

Innate immunity and susceptibility/protection in congenital CMV infection
Immune effector	Maternal/placental/fetal compartment	Proposed effect on CMV transmission/disease
NK cells-CD56^bright	Maternal (pregnancy); Uterine NK cells	(i) Decreased cytolytic potential; (ii) Increased risk of CMV transmission?
NK cells-NKG2C+	Fetal compartment	(i) Expansion of this NK subset in congenital and perinatal CMV; (ii) Correlation with symptomatic CMV disease?
Phagocytic cells	Placental compartment	(i) Neutrophils: possible role in defense; (ii) Macrophage: potentiates spread to syncytiotrophoblasts?
Toll-like receptors	Maternal compartment; Placental compartment	(i) TLR2 polymorphism; ↓ signaling to CMV glycoproteins; ↑ risk of CMV disease in transplant patients; increased transmission risk?; (ii) TLR3 polymorphism; decreased signaling to CMV antigens; (iii) TLR7 polymorphism: decreased antibody response to glycoprotein B?
Cytokines Chemokines Defensins	Neonatal compartment; Maternal compartment; Placental compartment; Placental-fetal interface	(i) ↑ IL-8 ↓ IF-𝛾 may correlate with increased transmission risk; (ii) Increased maternal CCL-10 correlates with transmission; (iii) Increased placental MCP-1 expression correlates with fetal demise; (iv) Physiological increase in uterine IL-10 in pregnancy: increased risk of reactivation/transmission?; (v) Beta-defensins 8 and 31 proposed to be upregulated in amniotic fluid of asymptomatically congenitally infected infants